dc.contributor.author | Elkington, P.T. | |
dc.contributor.author | Ugarte Gil, Cesar Augusto | |
dc.contributor.author | Friedland, J.S. | |
dc.date.accessioned | 2022-01-18T19:34:35Z | |
dc.date.available | 2022-01-18T19:34:35Z | |
dc.date.issued | 2011 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12866/11034 | |
dc.description.abstract | Tuberculosis (TB) remains a global health pandemic. Infection is spread by the aerosol route and Mycobacterium tuberculosis must drive lung destruction to be transmitted to new hosts. Such inflammatory tissue damage is responsible for morbidity and mortality in patients. The underlying mechanisms of matrix destruction in TB remain poorly understood but consideration of the lung extracellular matrix predicts that matrix metalloproteinases (MMPs) will play a central role, owing to their unique ability to degrade fibrillar collagens and other matrix components. Since we proposed the concept of a matrix degrading phenotype in TB a decade ago, diverse data implicating MMPs as key mediators in TB pathology have accumulated. We review the lines of investigation that have indicated a critical role for MMPs in TB pathogenesis, consider regulatory pathways driving MMPs and propose that inhibition of MMP activity is a realistic goal as adjunctive therapy to limit immunopathology in TB. ERS . | en_US |
dc.language.iso | eng | |
dc.publisher | European Respiratory Society | |
dc.relation.ispartofseries | European Respiratory Journal | |
dc.rights | info:eu-repo/semantics/restrictedAccess | |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es | |
dc.subject | Humans | en_US |
dc.subject | pathology | en_US |
dc.subject | genetics | en_US |
dc.subject | metabolism | en_US |
dc.subject | phenotype | en_US |
dc.subject | protein expression | en_US |
dc.subject | pathogenicity | en_US |
dc.subject | morbidity | en_US |
dc.subject | review | en_US |
dc.subject | mortality | en_US |
dc.subject | Mycobacterium tuberculosis | en_US |
dc.subject | Tuberculosis | en_US |
dc.subject | enzymology | en_US |
dc.subject | interstitial collagenase | en_US |
dc.subject | Monocytes | en_US |
dc.subject | lung tuberculosis | en_US |
dc.subject | Tuberculosis, Pulmonary | en_US |
dc.subject | doxycycline | en_US |
dc.subject | immunoglobulin G | en_US |
dc.subject | enzyme activity | en_US |
dc.subject | radiography | en_US |
dc.subject | BCG vaccine | en_US |
dc.subject | pathogenesis | en_US |
dc.subject | enzyme inhibition | en_US |
dc.subject | immune reconstitution inflammatory syndrome | en_US |
dc.subject | dexamethasone | en_US |
dc.subject | prediction | en_US |
dc.subject | Lung | en_US |
dc.subject | drug antagonism | en_US |
dc.subject | bacterial transmission | en_US |
dc.subject | CD14 antigen | en_US |
dc.subject | collagen fibril | en_US |
dc.subject | drug targeting | en_US |
dc.subject | enzyme degradation | en_US |
dc.subject | Extracellular Matrix | en_US |
dc.subject | gelatinase A | en_US |
dc.subject | gelatinase B | en_US |
dc.subject | Gene Expression Profiling | en_US |
dc.subject | Immunopathology | en_US |
dc.subject | matrilysin | en_US |
dc.subject | matrix metalloproteinase inhibitor | en_US |
dc.subject | Matrix Metalloproteinases | en_US |
dc.subject | neutrophil collagenase | en_US |
dc.subject | stromelysin | en_US |
dc.subject | stromelysin 2 | en_US |
dc.subject | toll like receptor | en_US |
dc.subject | tuberculous meningitis | en_US |
dc.title | Series "matrix metalloproteinases in lung health and disease": Matrix metalloproteinases in tuberculosis | en_US |
dc.type | info:eu-repo/semantics/review | |
dc.identifier.doi | https://doi.org/10.1183/09031936.00015411 | |
dc.subject.ocde | https://purl.org/pe-repo/ocde/ford#3.02.07 | |
dc.relation.issn | 1399-3003 |
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